About OU Medicine

At OU Medicine, our mission is leading health care. Our vision is to be the premiere enterprise for advancing health care, medical education and research for the community, state and region. Through our combined efforts we strive to improve the lives of all people.

Children's Services

Education & Research

The College of Medicine is the largest component of the University of Oklahoma Health Sciences Center and is at the center of OU Medicine. Our mission is leading health care - in education, research and patient care.

Easing the Heartache

When John Wesley "electrocuted" a patient to treat angina 225 years ago, "the violent symptoms immediately ceased, and he fell into a sweet sleep." The Methodism founder and amateur physician felt he was onto something, but what? Today, OU physiologists are leading international efforts to explain the unsolved mystery of how electrical stimulation can eliminate the pain of chronic angina.

Anyone who has experienced angina knows one thing for certain: it lives up to its name.

Angina comes from the Latin angerer, which means to strangle - an apt description for the choking, suffocating pain that results when the heart isn't receiving all the oxygen it needs, a condition called ischemia.

It can occur during exercise or emotional stress when the heart needs extra oxygen or it can result from a restriction in blood flow. This ischemic pain is the manifestation of coronary artery disease and a wake up call to the brain that the heart is in trouble.

While the signal answers one question for the sufferer - "yes, you are in danger of having a heart attack" - it poses many other ones for a neurophysiologist like Robert D. Foreman, Ph.D., chair of the Department of Physiology.

Where does the pain originate? Why do people say they're having chest pain and not heart pain? Why does electrical stimulation of the spine alleviate pain for people with end-stage coronary heart disease or refractory angina? And how does this same electrical stimulation appear to have the ability to protect the heart?

Foreman's interest in pain and heart disease is decades old and personal in origin. He was 19 and moving heavy pallets of paint at a factory in his home town of Orange City, Iowa, when the brakes on his forklift failed. The machine tipped over the edge of a loading dock, crushing and nearly severing Foreman's left arm. The arm was successfully reattached, but he spent a year in and out of a hospital in painful recuperation.

Foreman says the experience triggered an interest in science and led him to Loyola University's Stritch School of Medicine in Chicago, where he earned a Ph.D. in physiology in 1973, and a postdoctoral fellowship at the Marine Biomedical Institute of the University of Texas' medical branch in Galveston.

Meanwhile, his father underwent heart surgery, further stimulating Foreman's interest in heart disease. He became determined to find an answer in the nervous system that explains why and how our brains hear "chest" or "arm" but not "heart" when it's our heart that's in trouble.

By the mid-80's, Foreman had discovered proof that the spinothalmic tract is the pathway used to take messages from excited neurons in the heart and relay them to the brain. He was also able to show that this pathway is the same one that carries painful information to the brain from the muscles and skin that overlay the heart. When messages from the heart are sent, the brain, unaccustomed to receiving pain signals from the heart, misinterprets the point of origin as "chest" or "arm."

More recently, Foreman made the surprising discovery that the vagus nerve, the longest of the cranial nerves, delivers information about angina pain as well.

It has long been known that information about the heart is delivered to the spinal cord and then to the brain at the thoracic vertebrae T1 to T5. However, Foreman and his OU research team have recently demonstrated that information from the heart also arrives at the cervical C1 and C2 spinal cord.

More important, "we've discovered that if we excite cells in C1 and C2, it can modulate or turn off painful input to T1 and T5," Foreman said. "We believe it modulates activity all the way down the spinal cord."

Foreman and an international research group of physicians and scientists he formed in 1996 have also discovered that the use of electrical spinal cord stimulation in the T1 to T5 as well as the C1 and C2 region can not only reduce pain, but also may protect the heart itself.

Spinal cord stimulation (SCS) has long been used at T1 to treat angina patients in Europe. For almost all patients, the pain stops immediately, Foreman said.

"Relief comes very quickly for these patients, who come in unable to walk for more than two yards without overwhelming chest pain," Foreman said. "The physician inserts the device, gets it placed right, and within 30 seconds they are rid of their pain." He quoted a Dutch colleague as saying that some patients begin crying with relief.

As wonderful as pain elimination is for these patients, something more is also going on, Foreman said.

"We also see improvement in how the heart works. For example, there is increased exercise capacity in that the patients can walk farther. Is the heart getting more oxygen? That's what we're hoping to find out." One clue already discovered is that when SCS is used, there is a corresponding reduction in the lactate production that occurs when the heart isn't receiving enough oxygen.

Another of Foreman's basic research studies shows that when SCS is applied for 15 minutes prior to blocking an artery for 30 minutes, the infarction, or destroyed area of the heart, is significantly smaller than it is in animals where an artery was blocked but no SCS was used.

How does it work? SCS may trigger a beneficial neurochemical reaction, Foreman says. "Are there changes in the chemicals being released? Do we change how the blood is distributed in the heart?

"We know that the nervous system of the heart operates on impulses of electricity. We can take a tiny, tiny electrode and get it near a cell and record the electrical activity. You can see those impulses going boom, boom, boom, boom.

"If I pinch a coronary artery to stop blood flow, then this activity impulse gets very, very active, and you see lots of these impulses. We know that one way the nervous system gets information is from frequencies, so with more of these impulses, you get the alarm system. You want the warning, you want the alarm system and you want the protection. But if it goes wrong, you have continual pain.

"What I've seen with the (SCS) device is this: If I have it sitting on the spinal cord with electricity going in and then I pinch an artery, I'll see very few impulses. It stabilizes or suppresses the cardiac neural activity."

Foreman said another positive aspect of SCS is that it doesn't mask the body's "alarm system," only the chronic pain of refractory angina.

His goal is to provide a complete physiological explanation of why SCS influences the heart the way it does. "All we know now is that it works," he said.